scholarly journals Crosstalk between G protein-coupled receptors (GPCRs) and tyrosine kinase receptor (TXR) in the heart after morphine withdrawal

2013 ◽  
Vol 4 ◽  
Author(s):  
Pilar Almela ◽  
Juan-Antonio García-Carmona ◽  
Elena Martínez-Laorden ◽  
María-Victoria Milanés ◽  
María-Luisa Laorden
Keyword(s):  
Tyrosine Kinase ◽  
G Protein ◽  
G Protein Coupled Receptors ◽  
Morphine Withdrawal ◽  
Tyrosine Kinase Receptor ◽  
G Protein Coupled

Regulation of tyrosine kinase cascades by G-protein-coupled receptors

1999 ◽  
Vol 11 (2) ◽  
pp. 177-183 ◽  
Author(s):  
Louis M Luttrell ◽  
Yehia Daaka ◽  
Robert J Lefkowitz
Keyword(s):  
Tyrosine Kinase ◽  
G Protein ◽  
G Protein Coupled Receptors ◽  
G Protein Coupled

scholarly journals Role of Protein Kinase C, PI3-kinase and Tyrosine Kinase in Activation of MAP Kinase by Glucose and Agonists of G-protein Coupled Receptors in INS-1 Cells

2001 ◽  
Vol 2 (3) ◽  
pp. 233-244 ◽  
Author(s):  
Dietmar Böcker ◽  
Eugen J. Verspohl
Keyword(s):  
Protein Kinase ◽  
Tyrosine Kinase ◽  
Map Kinase ◽  
G Protein ◽  
Kinase Activity ◽  
Kinase Inhibitor ◽  
Pi3 Kinase ◽  
G Protein Coupled Receptors ◽  
Kinase C ◽  
G Protein Coupled

MAP (mitogen-activated protein) kinase (also called Erk 1/2) plays a crucial role in cell proliferation and differentiation. Its impact on secretory events is less well established. The interplay of protein kinase C (PKC), PI3-kinase nd cellular tyrosine kinase with MAP kinase activity using inhibitors and compounds such as glucose, phorbol 12-myristate 13-acetate (PMA) and agonists of G-protein coupled receptors like gastrin releasing peptide (GRP), oxytocin (OT) and glucose-dependent insulinotropic peptide (GIP) was investigated in INS-1 cells, an insulin secreting cell line. MAP kinase activity was determined by using a peptide derived from the EGF receptor as a MAP kinase substrate and [P32]ATP. Glucose as well as GRP, OT and GIP exhibited a time-dependent increase in MAP kinase activity with a maximum at time point 2.5 min. All further experiments were performed using 2.5 min incubations. The flavone PD 098059 is known to bind to the inactive forms of MEK1 (MAPK/ERK-Kinase) thus preventing activation by upstream activators. 20 μM PD 098059 (IC50=51 μM) inhibited MAP kinase stimulated by either glucose, GRP, OT, GIP or PMA. Inhibiton (“downregulation”) of PKC by a long term (22h) pretreatment with 1 μM PMA did not influence MAP kinase activity when augmented by either of the above mentioned compound. To investigate whether PI3-kinase and cellular tyrosine kinase are involved in G-protein mediated effects on MAP kinase, inhibitors were used: 100 nM wortmannin (PI3-kinase inhibitor) reduced the effects of GRP, OT and GIP but not that of PMA; 100 μM genistein (tyrosine kinase inhibitor) inhibited the stimulatory effect of either above mentioned compound on MAP kinase activation. Inhibition of MAP kinase by 20 μM PD 098059 did not influence insulin secretion modulated by either compound (glucose, GRP, OT or GIP). [H3]Thymidine incorporation, however, was severely inhibited by PD 098059. Thus MAP kinase is important for INS-1 cell proliferation but not for its insulin secretory response with respect to major initiators and modulators of insulin release. The data indicate that MAP kinase is active and under the control of MAP kinase. PKC is upstream of a genisteinsensitive tyrosine kinase and probably downstream of a PI3-kinase in INS-1 cells.

Aequorin-Based Functional Assays for G-Protein-Coupled Receptors, Ion Channels, and Tyrosine Kinase Receptors

2002 ◽  
Vol 8 (5-6) ◽  
pp. 319-330 ◽  
Author(s):  
Vincent J. Dupriez ◽  
Karlien Maes ◽  
Emmanuel Le Poul ◽  
Emmanuel Burgeon ◽  
Michel Detheux
Keyword(s):  
Ion Channels ◽  
Tyrosine Kinase ◽  
G Protein ◽  
G Protein Coupled Receptors ◽  
Tyrosine Kinase Receptors ◽  
Functional Assays ◽  
G Protein Coupled
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